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Colorectal and Prostate Cancer Risk in Diabetes: Metformin, an Actor behind the Scene.

Anwar MA, Kheir WA, Eid S, Fares J, Liu X, Eid AH, Eid AA - J Cancer (2014)

Bottom Line: Epidemiological studies provide strong evidence that subjects with diabetes are at significantly higher risk of developing many forms of cancer and especially solid tumors.In addition to pancreatic and breast cancer, the incidence of colorectal cancer and prostate cancer is increased in type 2 diabetes.We review the role of AMPK activation in autophagy, oxidative stress, inflammation, apoptosis, and cell cycle progression.

View Article: PubMed Central - PubMed

Affiliation: 1. Department of Biological and Environmental Sciences, College of Arts and Sciences, Qatar University, Doha - Qatar;

ABSTRACT
Both diabetes and cancer are prevalent diseases whose incidence rates are increasing worldwide, especially in countries that are undergoing rapid industrialization changes. Apparently, lifestyle risk factors including diet, physical inactivity and obesity play pivotal, yet preventable, roles in the etiology of both diseases. Epidemiological studies provide strong evidence that subjects with diabetes are at significantly higher risk of developing many forms of cancer and especially solid tumors. In addition to pancreatic and breast cancer, the incidence of colorectal cancer and prostate cancer is increased in type 2 diabetes. While diabetes (type 2) and cancer share many risk factors, the biological links between the two diseases are poorly characterized. In this review, we highlight the mechanistic pathways that link diabetes to colorectal and prostate cancer and the use of Metformin, a diabetes drug, to prevent and/or treat colorectal and prostate cancer. We review the role of AMPK activation in autophagy, oxidative stress, inflammation, apoptosis, and cell cycle progression.

No MeSH data available.


Related in: MedlinePlus

Metformin-mediated amelioration in diabetic and cancerous deranged metabolic profile, improvements in hemostasis and endothelial function, with regression of proliferative state. Metformin acts primarily on the liver and reduces glucose output, and secondarily on the peripheral tissues to increase glucose uptake. By decreasing gluconeogenesis, it ameliorates hyperglycemia in type 2 diabetes, improves endothelial function, oxidative stress, insulin resistance and fat redistribution. Accumulating evidence supports the antiproliferative role of metformin in colon and prostate cancer.
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Figure 1: Metformin-mediated amelioration in diabetic and cancerous deranged metabolic profile, improvements in hemostasis and endothelial function, with regression of proliferative state. Metformin acts primarily on the liver and reduces glucose output, and secondarily on the peripheral tissues to increase glucose uptake. By decreasing gluconeogenesis, it ameliorates hyperglycemia in type 2 diabetes, improves endothelial function, oxidative stress, insulin resistance and fat redistribution. Accumulating evidence supports the antiproliferative role of metformin in colon and prostate cancer.

Mentions: The history of metformin, a biguanide derivative, dates back to the Middle-Ages, and its structural analogue galegine was isolated from Galega officinalis (goat's rue, French lilac, Italian fitch); a plant native to the Middle East that has been used for treatment of diabetes in Europe 13. Accumulating evidence shows beneficial survival effects of therapeutic intervention with metformin for cancer patients with T2DM (Fig. 1). Metformin, a cationic (hydrophilic base) drug, exerts its pleiotropic pharmacological effects beyond those of metabolic control 14, and includes favorable anti-inflammatory outcomes 15, 16.


Colorectal and Prostate Cancer Risk in Diabetes: Metformin, an Actor behind the Scene.

Anwar MA, Kheir WA, Eid S, Fares J, Liu X, Eid AH, Eid AA - J Cancer (2014)

Metformin-mediated amelioration in diabetic and cancerous deranged metabolic profile, improvements in hemostasis and endothelial function, with regression of proliferative state. Metformin acts primarily on the liver and reduces glucose output, and secondarily on the peripheral tissues to increase glucose uptake. By decreasing gluconeogenesis, it ameliorates hyperglycemia in type 2 diabetes, improves endothelial function, oxidative stress, insulin resistance and fat redistribution. Accumulating evidence supports the antiproliferative role of metformin in colon and prostate cancer.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4216797&req=5

Figure 1: Metformin-mediated amelioration in diabetic and cancerous deranged metabolic profile, improvements in hemostasis and endothelial function, with regression of proliferative state. Metformin acts primarily on the liver and reduces glucose output, and secondarily on the peripheral tissues to increase glucose uptake. By decreasing gluconeogenesis, it ameliorates hyperglycemia in type 2 diabetes, improves endothelial function, oxidative stress, insulin resistance and fat redistribution. Accumulating evidence supports the antiproliferative role of metformin in colon and prostate cancer.
Mentions: The history of metformin, a biguanide derivative, dates back to the Middle-Ages, and its structural analogue galegine was isolated from Galega officinalis (goat's rue, French lilac, Italian fitch); a plant native to the Middle East that has been used for treatment of diabetes in Europe 13. Accumulating evidence shows beneficial survival effects of therapeutic intervention with metformin for cancer patients with T2DM (Fig. 1). Metformin, a cationic (hydrophilic base) drug, exerts its pleiotropic pharmacological effects beyond those of metabolic control 14, and includes favorable anti-inflammatory outcomes 15, 16.

Bottom Line: Epidemiological studies provide strong evidence that subjects with diabetes are at significantly higher risk of developing many forms of cancer and especially solid tumors.In addition to pancreatic and breast cancer, the incidence of colorectal cancer and prostate cancer is increased in type 2 diabetes.We review the role of AMPK activation in autophagy, oxidative stress, inflammation, apoptosis, and cell cycle progression.

View Article: PubMed Central - PubMed

Affiliation: 1. Department of Biological and Environmental Sciences, College of Arts and Sciences, Qatar University, Doha - Qatar;

ABSTRACT
Both diabetes and cancer are prevalent diseases whose incidence rates are increasing worldwide, especially in countries that are undergoing rapid industrialization changes. Apparently, lifestyle risk factors including diet, physical inactivity and obesity play pivotal, yet preventable, roles in the etiology of both diseases. Epidemiological studies provide strong evidence that subjects with diabetes are at significantly higher risk of developing many forms of cancer and especially solid tumors. In addition to pancreatic and breast cancer, the incidence of colorectal cancer and prostate cancer is increased in type 2 diabetes. While diabetes (type 2) and cancer share many risk factors, the biological links between the two diseases are poorly characterized. In this review, we highlight the mechanistic pathways that link diabetes to colorectal and prostate cancer and the use of Metformin, a diabetes drug, to prevent and/or treat colorectal and prostate cancer. We review the role of AMPK activation in autophagy, oxidative stress, inflammation, apoptosis, and cell cycle progression.

No MeSH data available.


Related in: MedlinePlus